[Federal Register Volume 68, Number 26 (Friday, February 7, 2003)]
[Notices]
[Page 6493]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 03-2989]


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DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health


Government-Owned Inventions; Availability for Licensing

AGENCY: National Institutes of Health, Public Health Service, DHHS.

ACTION: Notice.

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SUMMARY: The inventions listed below are owned by agencies of the U.S. 
Government and are available for licensing in the U.S. in accordance 
with 35 U.S.C. 207 to achieve expeditious commercialization of results 
of federally-funded research and development. Foreign patent 
applications are filed on selected inventions to extend market coverage 
for companies and may also be available for licensing.

ADDRESSES: Licensing information and copies of the U.S. patent 
applications listed below may be obtained by writing to the indicated 
licensing contact at the Office of Technology Transfer, National 
Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, 
Maryland 20852-3804; telephone: (301) 496-7057; fax: (301) 402-0220. A 
signed Confidential Disclosure Agreement will be required to receive 
copies of the patent applications.

Recombinant SUMO-1 Isopeptidase Substrates for FRET Assays

Mary Dasso and Jun Hang (NICHD).
DHHS Reference No. E-086-02/0--Research Tool.
Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; 
[email protected].

    The NIH announces a new Fluorescence Resonance Energy Transfer 
(FRET) assay for peptidases that regulate the processing of SUMO-1 and 
its removal from conjugation. SUMO-1 is an ubiquitin-like protein that 
becomes covalently linked to other proteins, which in turn may 
participate in events leading to cancer and viral infection. The 
inventors have created a FRET substrate that fuses unprocessed SUMO-1 
at its N- and C-termini with different Green Fluorescence Protein (GFP) 
derivatives. The FRET assay may be used to identify pharmacological 
agents that can regulate the SUMO-1 peptidases or to monitor their 
activities.

Human Gene Critical to Fertility

Lawrence Nelson and Zhi-bin Tong (NICHD).
DHHS Reference No. E-239-00/1 filed 04 Apr 2001 (PCT/US01/10981).
Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; 
[email protected].

    Some molecular pathways are unique to the reproductive process. 
Illuminating such processes would be expected to lead the way to the 
most specific molecular contraceptive targets. The Mater gene is 
essential for embryonic development beyond the two-cell stage. Mater 
expression is specific to the oocyte. Thus, Mater appears to qualify as 
a player in a unique molecular pathway that is specific to the 
reproductive process.
    The human MATER gene was identified through research investigating 
autoimmune premature ovarian failure. Premature ovarian failure (POF) 
is a term used to describe a condition associated with female sex 
hormone deficiency and infertility in women younger than age 40. As 
many as 1% of all women in the United States are thought to be 
afflicted with POF. Autoimmunity is a well-established mechanism of 
premature ovarian failure.
    The NIH announces a new technology that encompasses the MATER gene, 
protein and MATER-specific antibodies. These molecules can be used in 
diagnosing and/or treating infertility, and in developing 
contraceptives.

Anti-Inflammatory Actions of Cytochrome P450 Epoxygenase-derived 
Eicosanoids

Drs. Darryl C. Zeldin (NIEHS), James Liao (EM).
DHHS Reference Nos. E-252-1999/0-US-02 filed 09 Aug 2000 and E-252-
1999/0-PCT-03 filed 10 Aug 2000.
Licensing Contact: Marlene Shinn-Astor; (301) 435-4426; 
[email protected].

    Cytochrome P450s catalyze the NADPH-dependent oxidation of 
arachidonic acid to various eicosanoids found in several species 
including humans. The eicosanoids are biosynthesized in numerous 
tissues including pancreas, intestine, kidney, heart, and lung where 
they are involved in many different biological activities.
    The NIH announces a new therapy wherein epoxyeicosatrienoic acid 
(EET) compositions have been found to be useful in preventing 
endothelial cell death due to hypoxia-reoxygenation. Given that 
endothelial injury is an important early event in the development of 
the atherosclerotic plaque and is associated with myocardial 
dysfunction in ischemic heart disease, reduced EET levels are 
speculated to be involved in the pathogenesis of these cardiovascular 
disorders.
    This research is described in Yang et al., Molecular Pharmacology 
60: 310-320, 2001.

    Dated: January 29, 2003.
Jack Spiegel,
Director, Division of Technology, Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 03-2989 Filed 2-6-03; 8:45 am]
BILLING CODE 4140-01-P